PMID- 21654754
OWN - NLM
STAT- MEDLINE
DCOM- 20120110
LR  - 20161125
IS  - 1348-4214 (Electronic)
IS  - 0916-9636 (Linking)
VI  - 34
IP  - 9
DP  - 2011 Sep
TI  - Endothelial progenitor cells relationships with clinical and biochemical factors 
      in a human model of blunted angiotensin II signaling.
PG  - 1017-22
LID - 10.1038/hr.2011.72 [doi]
AB  - Angiotensin II (Ang II) is essential for endothelial progenitor cells (EPCs) 
      function as Ang-II-induced oxidative stress causes senescence of EPCs and 
      endothelial dysfunction and Ang II type 1 receptor blockers increase EPCs. 
      Moreover, EPCs activity is dependent on nitric oxide (NO) and heme oxygenase 
      (HO)-1 as these correlate with EPCs senescence and are reduced in hypertensives. 
      Bartter's/Gitelman's syndrome patients (BS/GS), have increased Ang II yet 
      normo/hypotension along with blunted Ang II signaling, reduced oxidative stress, 
      increased NO and HO-1, thus presenting a unique system to explore EPC biology and 
      its relationship with vascular clinical and biochemical correlates. Circulating 
      EPCs, NO-dependent vasodilation (flow-mediated dilation (FMD)) and HO-1 gene 
      expression were characterized in 10 BS/GS patients and in 10 normotensive 
      subjects. EPCs defined by cell surface antigens CD34+kinase-insert domain 
      receptor (KDR+), CD133+KDR+ and CD133+CD34+KDR+ cells were quantitiated via 
      direct three-color flow-cytometry analysis, HO-1 gene expression by reverse 
      transcription-PCR and FMD by B-mode echo scan of the right brachial artery. 
      Correlation analysis was carried out regarding FMD and EPCs, FMD and HO-1 and 
      EPCs and HO-1. In BS/GS, CD34+KDR+ cell numbers did not differ from controls 
      while CD133+KDR+ and CD133+CD34+KDR+ cell numbers were higher. HO-1 gene 
      expression, as well as FMD, was higher in BS/GS compared with controls. Both 
      CD133+KDR+ and CD133+CD34+KDR+ strongly correlated with both FMD and HO-1. FMD 
      and HO-1 were also strongly correlated. These results document in a human system 
      that EPC numbers and specific populations are related to important clinical and 
      biochemical factors involved in cardiovascular (CV) status and reaffirm the 
      utility of BS/GS patients as a useful system to investigate EPC's role(s) in the 
      pathophysiology of cardiovascular remodeling in humans.
FAU - Calo, Lorenzo A
AU  - Calo LA
AD  - Department of Clinical and Experimental Medicine, Clinica Medica 4, School of 
      Medicine, University of Padova, Padova, Italy. renzcalo@unipd.it
FAU - Facco, Monica
AU  - Facco M
FAU - Davis, Paul A
AU  - Davis PA
FAU - Pagnin, Elisa
AU  - Pagnin E
FAU - Maso, Lucia Dal
AU  - Maso LD
FAU - Puato, Massimo
AU  - Puato M
FAU - Caielli, Paola
AU  - Caielli P
FAU - Agostini, Carlo
AU  - Agostini C
FAU - Pessina, Achille C
AU  - Pessina AC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110609
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (AC133 Antigen)
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, CD34)
RN  - 0 (Glycoproteins)
RN  - 0 (PROM1 protein, human)
RN  - 0 (Peptides)
RN  - 11128-99-7 (Angiotensin II)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.14.18 (HMOX1 protein, human)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
SB  - IM
CIN - Hypertens Res. 2011 Sep;34(9):989-90. PMID: 21697851
MH  - AC133 Antigen
MH  - Adult
MH  - Angiotensin II/*physiology
MH  - Antigens, CD/physiology
MH  - Antigens, CD34/physiology
MH  - Bartter Syndrome/genetics/*physiopathology
MH  - Brachial Artery/physiology/physiopathology
MH  - Endothelial Cells/*physiology
MH  - Female
MH  - Gitelman Syndrome/genetics/*physiopathology
MH  - Glycoproteins/physiology
MH  - Heme Oxygenase-1/genetics/physiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nitric Oxide/physiology
MH  - Peptides/physiology
MH  - Signal Transduction
MH  - Stem Cells/*physiology
MH  - Vascular Endothelial Growth Factor Receptor-2/physiology
MH  - Vasodilation/physiology
EDAT- 2011/06/10 06:00
MHDA- 2012/01/11 06:00
CRDT- 2011/06/10 06:00
PHST- 2011/06/10 06:00 [entrez]
PHST- 2011/06/10 06:00 [pubmed]
PHST- 2012/01/11 06:00 [medline]
AID - hr201172 [pii]
AID - 10.1038/hr.2011.72 [doi]
PST - ppublish
SO  - Hypertens Res. 2011 Sep;34(9):1017-22. doi: 10.1038/hr.2011.72. Epub 2011 Jun 9.